Determining the effects of adrenaline and desflurane on QTc interval.

We read with great interest the article by Bestas et al1 entitled “The effect of adrenaline on desflurane-induced prolonged QTc interval: a randomized double-blind trial”, which is published in the current issue of European Review for Medical and Pharmacological Sciences. The Authors1 investigated the effect of adrenaline on desflurane-induced prolonged corrected QT (QTc) interval. They mentioned that adrenaline prolongs QT interval both in patients with long QT syndrome (LQTS) and in normal patients; and adrenaline QT stress test can be a beneficial tool in detecting LQTS in suspected cases. They concluded that desflurane caused progressive prolongation of the QTc interval, and adrenaline shortened QTc interval at application periods, due to increment in heart rate and ventricular contractility. Although, the current study is well-designed and gives detailed information, some comments may be of interest. Adrenaline activates slowly activating delayed rectifier potassium (IKs) channels responsible for repolarization, resulting in QT interval shortening in healthy individuals2. Provocative adrenaline QT stress testing can be resulted in a paradoxical gene specific response characterized by QT lengthening rather than expected shortening appears pathognomonic for individuals with KCNQ1 mutations (LQTS type 1)3. In patients with LQTS type 1 (LQTS1), unopposed depolarization via calcium (Ca2+) channels and sodium-calcium exchanger can be observed, resulting in QT interval lengthening3,4. Desflurane depresses the delayed outward potassium (K+) current associated with significant lengthening of QT interval5. In conclusion, adrenaline QT stress test can be a beneficial tool in unmasking concealed LQTS, particularly LQTS12. Adrenaline shortens QT interval in healthy individuals and prolongs in patients with LQTS12. Desflurane causes progressive prolongation of the QTc interval, as the authors mentioned, due to delayed outward K+current. Adrenaline shortens QTc interval due to not only increment in heart rate and ventricular contractility, but also activating IKs channels responsible for repolarization, as expectedly, contrary to authors’ sayings. Further electrophysiological studies are needed to determine the exact mechanism of QT shortening in co-administration of adrenaline and desflurane.